When testing the cranial nerves one must be cognizant of asymmetry. The following is a summary of the cranial nerves and their respective functioning.
Cranial Nerve I
Evaluate the patency of the nasal passages bilaterally by asking the patient to breath in through their nose while the examiner occludes one nostril at a time. Once patency is established, ask the patient to close their eyes. Occlude one nostril, and place a small bar of soap near the patent nostril and ask the patient to smell the object and report what it is. Making certain the patient's eyes remain closed. Switch nostrils and repeat. Furthermore, ask the patient to compare the strength of the smell in each nostril.
Very little localizing information can be obtained from testing the sense of smell. This part of the exam is often omitted, unless their is a reported history suggesting head trauma or toxic inhalation.
Cranial Nerve II
First test visual acuity by using a pocket visual acuity chart. Perform this part of the examination in a well lit room and make certain that if the patient wears glasses, they are wearing them during the exam. Hold the chart 14 inches from the patient's face, and ask the patient to cover one of their eyes completely with their hand and read the lowest line on the chart possible. Have them repeat the test covering the opposite eye. If the patient has difficulty reading a selected line, ask them to read the one above. Note the visual acuity for each eye.
Next evaluate the visual fields via confrontation. Face the patient one foot away, at eye level. Tell the patient to cover their right eye with their right hand and look the examiner in the eyes. Instruct the patient to remain looking you in the eyes and say "now" when the examiner's fingers enter from out of sight, into their peripheral vision. Once this is understood, cover your left eye with your left hand (the opposite eye of the patient) and extend your arm and first 2 fingers out to the side as far as possible. Beginning with your hand and arm fully extended, slowly bring your outstretched fingers centrally, and notice when your fingers enter your field of vision. The patient should say now at the same time you see your own fingers. Repeat this maneuver a total of eight times per eye, once for every 45 degrees out of the 360 degrees of peripheral vision. Repeat the same maneuver with the other eye.
Using an ophthalmoscope, observe the optic disc, physiological cup, retinal vessels and fovea. Note the pulsations of the optic vessels, check for a blurring of the optic disc margin and a change in the optic disc's color form its normal yellowish orange
The initial change in the ophthalmoscopic examination in a patient with increased intracranial pressure is the loss of pulsations of the retinal vessels. This is followed by blurring of the optic disc margin and possibly retinal hemorrhages.
Cranial Nerves II and III
Ask the patient to focus on an object in the distance. Observe the diameter of the pupils in a dimly lit room. Note the symmetry between the pupils. Next, shine the penlight or opthalmoscope light into one eye at a time and check both the direct and consensual light responses in each pupil. Note the rate of these reflexes. If they are sluggish or absent, test for pupillary constriction via accommodation by asking the patient to focus on the light pen itself while the examiner moves it closer and closer to their nose. Normally, as the eyes accommodate to the near object the pupils will constrict. The test for accomodation should also be completed in a dimly lit room. End the evaluation of cranial nerves II and III by observing the pupils in a well lit room and note their size and possible asymmetry.
Anisocoria is a neurological term indicating that one pupil is larger than another. Yet which pupil is abnormal? For example, if the right pupil is of a greater diameter than the left pupil in room light, is their a sympathetic lesion in the left eye or a parasympathetic lesion in the right eye? To determine this, observe and compare the asymmetry of the pupils in both bright and dim light. If the asymmetry is greatest in dim light than the sympathetic system is disrupted in the left eye, not allowing it to dilate in dim light, while the functioning right eye dilates even further in the dim light causing an increase in asymmetry. Conversely, if the asymmetry is greatest in bright light, then there is a parasympathetic lesion in the right eye. If the asymmetry remains the same in dim and bright light, then the anisocoria is physiologic.
Ptosis is the lagging of an eyelid. It has 2 distinct etiologies. Sympathetics going to the eye innervate Muller's muscle, a small muscle that elevates the eyelid. The III cranial nerve also innervates a much larger muscle that elevates the eye lid: the levator palpebrae. Thus, disruption of either will cause ptosis. The ptosis from a III nerve palsy is of greater severity than the ptosis due to a lesion of the sympathetic pathway, due to the size of the muscles innervated. As an aside, the parasympathetics run with the III cranial nerve and are usually affected with an abnormal III cranial nerve.
Anisocoria can only be produced if the efferent pathway of the pupillary light reflex is disrupted. A lesion of the afferent pathway along the II cranial does not yield anisocoria. To test for a lesion of the afferent pathway one must perform a "swinging light test". To interpret this test one must understand that the level of pupillary constriction is directly related to the total "perceived" illumination the brain appreciates from both eyes. If, for example, their is a 90% decrease in the afferent pathway in the left eye, shining a bright light in this eye will produce less constriction in both eyes (remember, the efferent pathways are functioning), compared to a bright light shining in the normal eye. Therefore with an afferent lesion, "swinging" the light back and forth between the eyes rapidly will cause the pupils to change diameter when the light goes from the normal eye (brain perceiving increased illumination) to the abnormal eye (brain perceiving less illumination). If both eyes are normal, no change would occur, because the total perceived illumination remains constant. This is called an afferent pupillary defect (APD) or Marcus-Gunn pupil.
Cranial Nerves III, IV and VI
Instruct the patient to follow the penlight or opthalmoscope with their eyes without moving their head. Move the penlight slowly at eye level, first to the left and then to the right. Then repeat this horizontal sweep with the penlight at the level of the patient's forehead and then chin. Note extra-ocular muscle palsies and horizontal or vertical nystagmus.
The limitation of movement of both eyes in one direction is called a conjugate lesion or gaze palsy, and is indicative of a central lesion. A gaze palsy can be either supranuclear (in cortical gaze centers) or nuclear (in brain stem gaze centers). If the gaze palsy is a nuclear gaze palsy, then the eyes can't be moved in the restricted direction voluntarily or by reflex, e.g. oculocephalic reflex. If the lesion is cortical, then only voluntary movement is absent and reflex movements are intact.
Disconjugate lesions, where the eyes are not restricted in the same direction or if only one eye is restricted, are due to more peripheral disruptions: cranial nerve nuclei, cranial nerves or neuromuscular junctions. One exception to this rule is an isolated impairment of adduction of one eye, which is commonly due to an ipsilateral median longitudinal fasciculus (MLF) lesion. This lesion is also called an internuclear ophthalmoplegia (INO). In INO, nystagmus is often present when the opposite eye is abducted.
Gaze-evoked nystagmus (nystagmus that is apparent only when the patient looks to the side or down) may be caused by many drugs, including ethanol, barbiturates, and phenytoin (Dilantin). Ethanol and barbiturates (recreational or therapuetic) are the most common cause of nystagmus. Dilantin may evoke nystagmus at slight overdoses, and opthalmoplegia at massive overdoses.
Abnormal patterns of eye movements may help localize lesions in the central nervous system. Ocular bobbing is the rhythmical conjugate deviation of the eyes downward. Ocular bobbing is without the characteristic rapid component of nystagmus. This movement is characteristic of damage to the pons.
Downbeat nystagmus (including a rapid component) may indicate a lesion compressing on the cervicomedullary junction such as a meningioma or chordoma.
An electronystagmogram (ENG) may be ordered to characterize abnormal eye movements. The basis of this test is that the there is an intrinsic dipole in each eyeball (the retina is negatively charged compared to the cornea. During an ENG, recording electrodes are placed on the skin around the eyes and the dipole movement is measured and eye movement is accurately characterized.
Cranial Nerve V
First, palpate the masseter muscles while you instruct the patient to bite down hard. Also note masseter wasting on observation. Next, ask the patient to open their mouth against resistance applied by the instructor at the base of the patient's chin.
Next, test gross sensation of the trigeminal nerve. Tell the patient to close their eyes and say "sharp" or "dull" when they feel an object touch their face. Allowing them to see the needle before this examination may alleviate any fear of being hurt. Using the needle and brush from your reflex hammer or the pin from a safety pin, randomly touch the patient's face with either the needle or the brush. Touch the patient above each temple, next to the nose and on each side of the chin, all bilaterally. Ask the patient to also compare the strength of the sensation of both sides. If the patient has difficulty distinguishing pinprick and light touch, then proceed to check temperature and vibration sensation using the vibration fork. One may warm it or cool it under a running faucet.
Finally, test the corneal reflex using a large Q-tip with the cotton extended into a wisp. Ask the patient to look at a distant object and then approaching laterally, touch the cornea (not the sclera) and look for the eye to blink. Repeat this on the other eye.
Some clinicians omit the corneal reflex unless there is sensory loss on the face as per history or examination, or if cranial nerve palsies are present at the pontine level.
Cranial Nerve VII
Initially, inspect the face during conversation and rest noting any facial asymmetry including drooping, sagging or smoothing of normal facial creases. Next, ask the patient to raise their eyebrows, smile showing their teeth, frown and puff out both cheeks. Note asymmetry and difficulty performing these maneuvers. Ask the patient to close their eyes strongly and not let the examiner pull them open. When the patient closes their eyes, simultaneously attempt to pull them open with your fingertips. Normally the patient's eyes cannot be opened by the examiner. Once again, note asymmetry and weakness.
When the whole side of the face is paralyzed the lesion is peripheral. When the forehead is spared on the side of the paralysis, the lesion is central (e.g., stroke). This is because a portion of the VII cranial nerve nucleus innervating the forehead receives input from both cerebral hemispheres. The portion of the VII cranial nerve nucleus innervating the mid and lower face does not have this dual cortical input.
Hyperacusis (increased auditory volume in an affected ear) may be produced by damage to the seventh cranial nerve. This is because the seventh cranial nerve innervates the stapedius muscle in the middle ear which damps ossicle movements which decreases volume. With seventh cranial nerve damage this muscle is paralyzed and hyperacusis occurs. Furthermore, since the branch of the seventh cranial nerve to the stapedius begins very proximally, hyperacusis secondary to seventh cranial nerve dysfunction indicates a lesion close to seventh cranial nerve's origin at the brainstem.
Cranial Nerve VIII
Assess hearing by instructing the patient to close their eyes and to say "left" or "right" when a sound is heard in the respective ear. Vigorously rub your fingers together very near to, yet not touching, each ear and wait for the patient to respond. After this test, ask the patient if the sound was the same in both ears, or louder in a specific ear. If there is lateralization or hearing abnormalities perform the Rinne and Weber tests using the 256 Hz tuning fork.
The Weber test is a test for lateralization. Wrap the tuning fork strongly on your palm and then press the butt of the instrument on the top of the patient's head in the midline and ask the patient where they hear the sound. Normally, the sound is heard in the center of the head or equally in both ears. If their is a conductive hearing loss present, the vibration will be louder on the side with the conductive hearing loss. If the patient doesn't hear the vibration at all, attempt again, but press the butt harder on the patient's head.
The Rinne test compares air conduction to bone conduction. Wrap the tuning fork firmly on your palm and place the butt on the mastoid eminence firmly. Tell the patient to say "now" when they can no longer hear the vibration. When the patient says "now", remove the butt from the mastoid process and place the U of the tuning fork near the ear without touching it. Tell the patient to say "now" when they can no longer hear anything. Normally, one will have greater air conduction than bone conduction and therefore hear the vibration longer with the fork in the air. If the bone conduction is the same or greater than the air conduction, there is a conductive hearing impairment on that side. If there is a sensineuronal hearing loss, then the vibration is heard substantially longer than usual in the air. Make certain that you perform both the Weber and Rinne tests on both ears. It would also be prudent to perform an otoscopic examination of both eardrums to rule out a severe otitis media, perforation of the tympanic membrane or even occlusion of the external auditory meatus, which all may confuse the results of these tests. Furthermore, if hearing loss is noted an audiogram is indicated to provide a baseline of hearing for future reference.
Because of the extensive bilateral connections of the auditory system, the only way to have an ipsilateral hearing loss is to have a peripheral lesion, i.e. at the cranial nerve nucleus or more peripherally. Bilateral hearing loss from a single lesion is invariably due to one located centrally.
Cranial Nerves IX and X
Ask the patient to swallow and note any difficulty doing so. Ask the patient if they have difficulty swallowing. Next, note the quality and sound of the patient's voice. Is it hoarse or nasal? Ask the patient to open their mouth wide, protrude their tongue, and say "AHH". While the patient is performing this task, flash your penlight into the patient's mouth and observe the soft palate, uvula and pharynx. The soft palate should rise symmetrically, the uvula should remain midline and the pharynx should constrict medially like a curtain. Often the palate is not visualized well during this manuever. One may also try telling the patient to yawn, which often provides a greater view of the elevated palate. Also at this time, use a tongue depressor and the butt of a long Q-tip to test the gag reflex. Perform this test by touching the pharynx with the instrument on both the left and then on the right side, observing the normal gag or cough.
Some clinicians omit testing for the gag reflex unless there is dysarthria or dysphagia present by history or examination, or if cranial nerve palsies are present at the medullary level.
Roughly 20% of normal individuals have a minimal or absent gag reflex.
Dysarthria and dysphagia are due to incoordination and weakness of the muscles innervated by the nucleus ambiguus via the IX and X cranial nerves. The severity of the dysarthria or dysphagia is different for single versus bilateral central lesions. The deficiency is often minor if the lesion is centrally located and in only one cortical hemisphere, because each nucleus ambiguus receives input from both crerebral hemispheres. In contrast, bilateral central lesions, or "pseudobulbar palsies", often produce marked deficits in phonation and swallowing. Furthermore, on examination the quality of the dysarthria is distinct for central versus peripheral lesions. Central lesions produce a strained, strangled voice quality, while peripheral lesions produce a hoarse, breathy and nasal voice.
Cranial Nerve XI
This cranial nerve is initially evaluated by looking for wasting of the trapezius muscles by observing the patient from the rear. Once this is done, ask the patient to shrug their shoulders as strong as they possible can while the examiner resists this motion by pressing down on the patient's shoulders with their hands. Next, ask the patient to turn their head to the side as strongly as they possibly can while the examiner once again resists with their hand.
Repeat this maneuver on the opposite side. The patient should normally overcome the resistance applied by the examiner. Note asymmetry.
Peripheral lesions produce ipsilateral sternocleidomastoid (SCM) weakness and ipsilateral trapezius weakness. Central lesions produce ipsilateral SCM weakness and contralateral trapezius weakness, because of differing sources of cerebral innervation. This is a common clinical misunderstanding.
Cranial Nerve XII
The hypoglossal nerve controls the intrinsic musculature of the tongue and is evaluated by having the patient "stick out their tongue" and move it side to side. Normally, the tongue will be protruded from the mouth and remain midline. Note deviations of the tongue from midline, a complete lack of ability to protrude the tongue, tongue atrophy and fasciculations on the tongue.
The tongue will deviate towards the side of a peripheral lesion, and to the opposite side of a central lesion.
|Special Topic: Pathology found on opthalmologic examination
||Papilledema. Note swelling of the disc, hemorrhages, and exudates, with preservation of the physiologic cup.
|Optic Atrophy. Note the chalky white disc with discrete margins. Optic atrophy is a late finding with increased intracranial pressure.
||Central Retinal Artery Occlusion. Note the diffusely pale retina and prominent central fovea which is usually blended in with the normal, pink retina.
|Central Retinal Vein Occlusion. The disc is massively swollen with diffuse hemorrhages and cotton-wool spots.
||Proliferative Diabetic Retinopathy. Note the multiple hemorrhages, exudates and neovascularization throughout the retina. Chorioretinal striae extend towards the area of fibrovascular proliferation in the lower portion of the photograph.
|Cytomegalovirus Retinitis. Note the area of retinal necrosis and hemorrhage along the lower portion of the photograph. Common in patinets with immunodeficiency, especially AIDS.